scholarly journals Chitosan Oligosaccharide Ameliorates Metabolic Syndrome Induced by Overnutrition via Altering Intestinal Microbiota

2021 ◽  
Vol 8 ◽  
Author(s):  
Yihua Wang ◽  
Shili Liu ◽  
Di Tang ◽  
Rui Dong ◽  
Qiang Feng
Keyword(s):  
Metabolic Syndrome ◽  
Gut Microbiota ◽  
Intestinal Microbiota ◽  
High Fat Diet ◽  
Lipid Lowering ◽  
Positive Interactions ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Clostridium Paraputrificum

Chitosan oligosaccharides (COS) play a prebiotic role in many ways, whereas its function on microbiota is not fully understood. In this study, the effects of COS on metabolic syndrome were initially investigated by testing changes in the physiological indicators after adding COS to the diet of mice with high fat (group H) and low fat (group L). The results showed that COS markedly inhibited the accumulation of body weight and liver fat induced by high-fat diet, as well as restored the elevated concentration of blood glucose and fasting insulin to normal levels. Next, changes of the murine intestinal microbiota were examined. The results exhibited that COS reduced with-in-sample diversity, while the between-sample microbial diversity enhanced. Specifically, COS enriched Clostridium paraputrificum and Clostridium ramosum in the mice on a high-fat diet, while the abundance of Clostridium cocleatum was reduced. As a comparison, Parabacteroides goldsteinii and Bacteroides uniformis increased their abundance in response to COS in the low-fat diet group. Noticeably, a large amount of Akkermansia muciniphila was enriched in both high-fat or low-fat diet groups. Among the differential fecal bacteria, Clostridium ramosume was found to be positively interacted with Faecalibacterim prausnitzii and Clostridium paraputrificum; Clostridium paraputrificum had a positive interactions with Lactococcus chungangensis and Bifidobacterium mongoliense, suggesting that COS probably ameliorate metabolic syndrome through the microbiota in view of the lipid-lowering effects of these interacted bacteria. Furthermore, the gene expression data revealed that COS improved the functions related to intestinal barrier and glucose transport, which could be the trigger and consequence of the variations in gut microbiota induced by COS. Additionally, correlation analysis found that intestinal bacteria are related to physiological parameters, which further supports the mediating role of gut microbiota in the beneficial effect of COS. In summary, our research results provide new evidence for the prebiotic effects of COS.

scholarly journals Effect of stevia on the gut microbiota and glucose tolerance in a murine model of diet-induced obesity

2020 ◽  
Vol 96 (6) ◽  
Author(s):  
Sarah L Becker ◽  
Edna Chiang ◽  
Anna Plantinga ◽  
Hannah V Carey ◽  
Garret Suen ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Gut Microbiota ◽  
Glucose Intolerance ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Treatment Groups ◽  
Low Fat Diet ◽  
Taxonomic Groups ◽  
Induced Changes

ABSTRACT Artificial sweeteners have been shown to induce glucose intolerance by altering the gut microbiota; however, little is known about the effect of stevia. Here, we investigate whether stevia supplementation induces glucose intolerance by altering the gut microbiota in mice, hypothesizing that stevia would correct high fat diet-induced glucose intolerance and alter the gut microbiota. Mice were split into four treatment groups: low fat, high fat, high fat + saccharin and high fat + stevia. After 10 weeks of treatment, mice consuming a high fat diet (60% kcal from fat) developed glucose intolerance and gained more weight than mice consuming a low fat diet. Stevia supplementation did not impact body weight or glucose intolerance. Differences in species richness and relative abundances of several phyla were observed in low fat groups compared to high fat, stevia and saccharin. We identified two operational taxonomic groups that contributed to differences in beta-diversity between the stevia and saccharin groups: Lactococcus and Akkermansia in females and Lactococcus in males. Our results demonstrate that stevia does not rescue high fat diet-induced changes in glucose tolerance or the microbiota, and that stevia results in similar alterations to the gut microbiota as saccharin when administered in concordance with a high fat diet.

scholarly journals Methionine Restriction Attenuates High-Fat Diet-Induced Gut-Brain Axis Circadian Rhythm Disorders and Cognitive Impairments (P08-052-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Luanfeng Wang ◽  
Bo Ren ◽  
Zhigang Liu ◽  
Xuebo Liu
Keyword(s):  
Metabolic Syndrome ◽  
Circadian Rhythm ◽  
High Fat Diet ◽  
Cognitive Impairments ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Methionine Restriction ◽  
Junction Protein ◽  
Circadian Rhythm Disorders

Abstract Objectives Methionine restriction (MR) has emerged as a promising dietary restriction on metabolic syndrome as its beneficial effects on increasing metabolic flexibility and up-regulating mitochondrial function. The circadian clock directs many aspects of metabolism and macronutrients can function as zeitgebers for the clock in a tissue-specific way. It has been demonstrated that high-fat diet could alter daily oscillations via gut-brain axis. We hypothesis that MR is a new strategy could reverse the high-fat diet induced circadian rhythm disorders and cognitive impairments. Methods 3 month-old male C57BL/6 J mice were assigned to four groups based on diet: low-fat diet (0.86% methionine), low-fat diet with MR(0.17% methionine), high-fat diet, and high-fat diet with MR. After 8 weeks treatment, we employed behavioral test, transmission electron microscope, and 16S rDNA sequencing to evaluate cognitive function, rhythmic variation and the interconnection between gut microbiota and central nervous system. Results MR diminished HFD-induced body weight gain and restored the glucose tolerance at ZT0 (light phase) and ZT12 (dark phase). The neuroprotective effects of MR were connected with the ERK/CREB/BDNF signaling pathway and synaptic plasticity. MR changed energy metabolism via activated mTOR/ULK/AMPK signaling in brain. MR ameliorated rhythmic oscillations of clock control gene Bmal1/Per2 in gut-brain axis. Moreover, MR attenuated HFD-induced intestinal inflammatory and protected gut barrier integrity via enhancing the expression of intestinal tight junction protein. The gut microbiome was re-shaped by MR treatment, accompanied by the alteration of short chain fatty acids, the microbial products mediating systemic metabolism and has benefits on brain function. MR increased microbiota-derived butyric and isovaleric which possible synchronizers of peripheral circadian clocks. Conclusions The present study provided comprehensive evidence that MR attenuated obesity-induced cognitive impairment via balancing the circadian rhythm in gut-brain axis and that is a potential new therapeutic avenue for treating metabolic syndrome-related neurodegenerative diseases. Funding Sources This work was financially supported by the National Key Research and Development Program of China, National Natural Science Foundation of China. Supporting Tables, Images and/or Graphs

scholarly journals Effect of a long-term high-protein diet on survival, obesity development, and gut microbiota in mice

2016 ◽  
Vol 310 (11) ◽  
pp. E886-E899 ◽  
Author(s):  
Pia Kiilerich ◽  
Lene Secher Myrmel ◽  
Even Fjære ◽  
Qin Hao ◽  
Floor Hugenholtz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Gut Microbiota ◽  
Dietary Fat ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Low Protein

Female C57BL/6J mice were fed a regular low-fat diet or high-fat diets combined with either high or low protein-to-sucrose ratios during their entire lifespan to examine the long-term effects on obesity development, gut microbiota, and survival. Intake of a high-fat diet with a low protein/sucrose ratio precipitated obesity and reduced survival relative to mice fed a low-fat diet. By contrast, intake of a high-fat diet with a high protein/sucrose ratio attenuated lifelong weight gain and adipose tissue expansion, and survival was not significantly altered relative to low-fat-fed mice. Our findings support the notion that reduced survival in response to high-fat/high-sucrose feeding is linked to obesity development. Digital gene expression analyses, further validated by qPCR, demonstrated that the protein/sucrose ratio modulated global gene expression over time in liver and adipose tissue, affecting pathways related to metabolism and inflammation. Analysis of fecal bacterial DNA using the Mouse Intestinal Tract Chip revealed significant changes in the composition of the gut microbiota in relation to host age and dietary fat content, but not the protein/sucrose ratio. Accordingly, dietary fat rather than the protein/sucrose ratio or adiposity is a major driver shaping the gut microbiota, whereas the effect of a high-fat diet on survival is dependent on the protein/sucrose ratio.

scholarly journals Altered Gut Microbiota Is a Novel Mechanism for the Adverse Effects Induced by Foodborne Titanium Dioxide Nanoparticles in Obese and Non-obese Mice (P21-021-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Hengjun Du ◽  
Xiaoqiong Cao ◽  
Yanhui Han ◽  
Min Gu ◽  
Hang Xiao
Keyword(s):  
Titanium Dioxide ◽  
Adverse Effects ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Obese Mice ◽  
High Fat ◽  
Low Fat ◽  
Colonic Inflammation ◽  
Tio2 Nps ◽  
Low Fat Diet

Abstract Objectives Many food products contain inorganic nanoparticles (NPs), such as titanium dioxide (TiO2) NPs. There is increasing concern about the potential unintended health risks associated with foodborne TiO2 NPs in certain populations, such as the obese. The purpose of this study was to determine the adverse effects of TiO2 NPs in obese individuals, the molecular mechanism involved and the potential role of gut microbiota in mediating the adverse effects. Methods Two types of TiO2 (30 nm and E171-Food grade TiO2) were mixed with mouse diet at 0.1 wt% and fed to two populations of mice (high-fat diet-fed obese mice and non-obese mice). Meanwhile, fecal samples from the above groups of mice were collected weekly for transplanting to four groups of mice fed a low-fat diet for 10 weeks. 16 s rRNA gene amplicon sequencing, histological analysis, immunohistochemistry, ELISA and SCFAs analysis were utilized to characterize the composition of the microbiota, inflammation status, and the effects of altered gut microbiota on the inflammation status of the mouse colon. Results TiO2 NPs significantly altered the composition of gut microbiota with stronger alterations in the high-fat diet-fed obese mice than the low-fat diet-fed non-obese mice. The abundance of inflammation-related cytokines (e.g., IL-10, IL-12p70, and IL-17) and myeloperoxidase (MPO) in the mouse colonic mucosa were significantly altered by TiO2 NPs to produce an inflammatory state. TiO2 NPs decreased the cecal levels of SCFAs such as butyrate. Moreover, the magnitude of the above alteration was higher in the obese mice than in the non-obese mice. After 10 weeks of microbial transplant, microbiota from the mice consuming a high-fat diet with TiO2 NPs led to an increase of pro-inflammatory cytokines, loss of healthy colonic morphology, and infiltration of immune cells in the colon of the low-fat diet-fed recipient mice, indicating a significant colonic inflammation. Conclusions TiO2 NPs altered gut microbiota in both obese and non-obese mice, with stronger effects in the obese mice, and the alteration of gut microbiota led to colonic inflammation in the mice. Overall, these findings provided a valuable new perspective on the potential adverse effects and appropriate mechanisms of foodborne TiO2 NPs among populations with different obese status. Funding Sources USDA/NIFA competitive grants to Hang Xiao.

scholarly journals THE ROLE OF THE INTESTINAL MICROBIOTA IN THE MODULATION OF FOOD INTAKE AND BODY WEIGHT

2017 ◽  
Author(s):  
Matthew John Dalby
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Intestinal Microbiota ◽  
High Fat Diet ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
Diet Induced Obesity

This research investigated the role of the intestinal microbiota in shaping host food intake and body weight through immunomodulation, the impact of refined and unrefined diets, and though fermentable fibre induced gastrointestinal hormone secretion. Gut-derived lipopolysaccharide activating TLR4 has been proposed to contribute to obesity. To investigate this, TLR4-/- or CD14-/- mice and C57BL/6J controls were fed a high-fat or low-fat diet. Neither TLR4-/- or CD14-/- were protected against high-fat diet-induced obesity. High-fat diet increased hypothalamic expression of SerpinA3N and SOCS3 regardless of genotype; however, inflammatory gene expression was not increased. To investigate the use of chow control diets in obesity-associated microbiota changes, C57BL/6J mice were fed a chow diet, refined high-fat, or low-fat diet. Both high-fat and low-fat refined diets resulted in similar dramatic alterations in the composition of the intestinal microbiota at the phylum, family, and species level compared to chow, while only high-fat diet feeding resulted in obesity and glucose intolerance. The roles of colonic GLP-1 and PYY in mediating fermentable fibre in reducing food intake and body fat were investigated using GLP-1R-/- and PYY-/- mice fed a high-fat diet supplemented with inulin or cellulose. Inulin supplementation reduced body fat and food intake in C57BL/6J control mice while GLP-1R-/- and PYY-/- mice showed an attenuated response to dietary inulin. In summary, this research questions the role of TLR4 and LPS in diet-induced obesity. These results demonstrate the importance of the control diet used in studies of obesity in mice and indicate that many of the obesity-associated changes in the gut microbiota are due to comparing refined high-fat diets with chow diets. These results also provide evidence for an essential role for both GLP-1 and PYY in mediating the food intake and bodyweight-reducing effects of fermentable fibre.

scholarly journals Berberine Relieves Metabolic Syndrome in Mice by Inhibiting Liver Inflammation Caused by a High-Fat Diet and Potential Association With Gut Microbiota

2022 ◽  
Vol 12 ◽  
Author(s):  
Jinjin Li ◽  
Jialin Li ◽  
Jiajia Ni ◽  
Caibo Zhang ◽  
Jianlei Jia ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
Inflammatory Response ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Liver Fat ◽  
Lipid Lowering ◽  
Inflammatory Factor ◽  
High Fat ◽  
Host Inflammatory Response ◽  
Microbiota Structure

Whether berberine mediates its anti-inflammatory and blood sugar and lipid-lowering effects solely by adjusting the structure of the gut microbiota or by first directly regulating the expression of host pro-inflammatory proteins and activation of macrophages and subsequently acting on gut microbiota, is currently unclear. To clarify the mechanism of berberine-mediated regulation of metabolism, we constructed an obese mouse model using SPF-grade C57BL/6J male mice and conducted a systematic study of liver tissue pathology, inflammatory factor expression, and gut microbiota structure. We screened the gut microbiota targets of berberine and showed that the molecular mechanism of berberine-mediated treatment of metabolic syndrome involves the regulation of gut microbiota structure and the expression of inflammatory factors. Our results revealed that a high-fat diet (HFD) significantly changed mice gut microbiota, thereby probably increasing the level of toxins in the intestine, and triggered the host inflammatory response. The HFD also reduced the proportion of short-chain fatty acid (SCFA)-producing genes, thereby hindering mucosal immunity and cell nutrition, and increased the host inflammatory response and liver fat metabolism disorders. Further, berberine could improve the chronic HFD-induced inflammatory metabolic syndrome to some extent and effectively improved the metabolism of high-fat foods in mice, which correlated with the gut microbiota composition. Taken together, our study may improve our understanding of host-microbe interactions during the treatment of metabolic diseases and provide useful insights into the action mechanism of berberine.

Polysaccharide from Flammulina velutipes Attenuates Markers of Metabolic Syndrome by modulating the Gut Microbiota and Lipid Metabolism in High fat Diet-fed Mice

2021 ◽  
Author(s):  
Ruiqiu Zhao ◽  
Yang Ji ◽  
Xin Chen ◽  
Qiuhui Hu ◽  
Liyan Zhao
Keyword(s):  
Metabolic Syndrome ◽  
Lipid Metabolism ◽  
Gut Microbiota ◽  
High Fat Diet ◽  
Flammulina Velutipes ◽  
Biological Macromolecules ◽  
High Fat

Natural biological macromolecules with putative functions of gut microbiota regulation possesses the advantage in improving metabolic syndrome (MS). In this research, we aimed to determine the effects of Flammulina velutipes...

Abstract 480: Exacerbation of Arterial Stiffness in Obese Adiponectin Deficient Mice

2015 ◽  
Vol 35 (suppl_1) ◽  
Author(s):  
Megha Murali ◽  
Carla Taylor ◽  
Peter Zahradka ◽  
Jeffrey Wigle
Keyword(s):  
Arterial Stiffness ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
High Fat Diet ◽  
Pulse Wave ◽  
High Fat ◽  
Low Fat ◽  
Low Fat Diet ◽  
High Fat Diets ◽  
Fat Diets

Background and Objective: Arterial stiffness is recognized as being an independent predictor of incipient vascular disease associated with obesity and metabolic syndrome. In obese subjects, the decrease in the plasma level of adiponectin, an anti-diabetic and anti-atherogenic adipokine, is well known. Hence the aim of our study was to examine the effect of loss of adiponectin on the development of arterial stiffness in response to a high fat diet. Methods and Results: Male 8-week old adiponectin knockout (APN KO) and C57BL/6 (control) mice were fed a high fat diet (60% Calories from fat) for 12 weeks to induce obesity and insulin resistance (n=10/group). APN KO and C57BL/6 mice were fed a low fat diet (10% Calories from fat) and used as lean controls (n=10/group). After 12 weeks on the high fat diet, the APN KO mice weighed significantly more than the C57BL/6 mice (45.1±1.3 g vs 40.1±1.1 g, p=0.0008) but there was no difference in the final weights between genotypes fed the low fat diet. APN KO mice on both high and low fat diets for 12 weeks developed insulin resistance as measured by oral glucose tolerance test (Area under curve (AUC) mmol/L х min = 437±70 and 438±57) as compared to the C57BL/6 mice fed low or high fat diets (AUC mmol/L х min = 251±27 and 245±43). Arterial stiffness was determined by Doppler pulse wave velocity analysis of the femoral artery. Pulse wave velocity was increased in APN KO mice fed a high fat diet relative to those fed the low fat diet (12.56±0.78 cm/s vs 9.47±0.95 cm/s, p=0.0035; n=8-10). Pulse wave velocity was not different between C57BL/6 control mice on the low or high fat diets (10.63±0.73 cm/s and 10.86±0.50 cm/s), thus revealing that only mice deficient in adiponectin developed arterial stiffness in response to high fat diet. Conclusions: Potentiation of the vascular stiffness in diet-induced obese APN KO mice indicates that adiponectin has a role in modulating vascular structure and the APN KO mouse models the vascular changes that occur in human obesity and metabolic disorders. Morphometric analysis of the aortic tissues for vessel thickness and expression of extracellular proteins will further validate the potential role of adiponectin on the maintenance of arterial elasticity in addition to its known effect on eNOS mediated vasoprotection.

scholarly journals Influence of gender on OVA-induced airway inflammation in C57/B6J mice on a high-fat diet

2018 ◽  
Vol 16 ◽  
pp. 205873921876094 ◽  
Author(s):  
Gang Yu ◽  
Lili Zhu ◽  
Haiyan Li ◽  
Youyou Shao ◽  
Lei Chong ◽  
...  
Keyword(s):  
Body Weight ◽  
High Fat Diet ◽  
Inflammatory Cells ◽  
Normal Weight ◽  
Male Mice ◽  
High Fat ◽  
Low Fat ◽  
Control Male ◽  
Low Fat Diet ◽  
Asthma Group

Overweight/obesity has been suggested as a risk factor for asthma development, and prospective studies have confirmed that high body weight precedes asthma symptoms. However, the nature of the association between overweight/obese status and asthma remains unclear. Animal models of obesity-related asthma are very useful for understanding disease pathophysiology. Although C57/B6J mice are the most widely used animal model for researching obesity-related asthma, gender differences are not always taken into consideration. Therefore, to explore the effect of gender on the development of obesity-related asthma, both female and male C57/B6J mice were used in this study. The mice were fed with a high-fat diet or a low-fat diet as control. Body weight, body length, liver weight, and Lee’s Index were used to evaluate obesity status, and lung histology, lung inflammatory cells infiltration, and inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined for asthma evaluation. We found that the mean body weight of male mice on a high-fat diet gradually increased and was significantly higher than control male mice on a low-fat diet ( P < 0.01), while no significant differences were found between female mice at the end of 12 weeks of feeding. Furthermore, the obese asthma group female and male mice exhibited significantly high inflammatory cells infiltration than normal weight or obese female and male mice ( P < 0.01). However, the obese asthma group presented higher Neu infiltration, Th1 cytokine, and interferon gamma (IFNγ) concentrations in BALF than the asthma group in both the genders ( P < 0.01). In conclusion, both female and male mice are suitable for the obesity-related asthma model, although male mice might be more stable. Besides, obesity-related asthma is not Th2 type asthma.

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